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  1. Jack Rusher is offline
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    Posted On:
    3/17/2010 4:56pm


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    Sorry in advance, I've not got most of my references in front of me.

    Quote Originally Posted by TheRuss View Post
    post-workout carbohydrate
    The research I've read suggests that there's no benefit in terms of protein synthesis (a long standing claim), but that post-workout carbs are good for recovery, including glycogen replacement, plus a spike in growth hormone and insulin. My preference here is non-fructose (which will only replenish liver glycogen, not muscle), with an especial fondness for starches that degrade to glucose (e.g. bananas in a smoothie).

    "Glycogen supercompensation occurs only when a low carbohydrate diet is combined with vigorous exercise followed by a high carbohydrate diet. Glycogen supercompensation occurs only in muscles that were trained and is maximal at a carbohydrate intake of approximately 25 grams per hour for average adults and possibly 40 grams or more per hour for bodybuilders."
    Glycogen Supercompensation Enhances Athletic Performance

    ... they make the point that it's not useful for power athletes because they're limited by other metabolic factors than glycogen. This is probably the case for fight day, but during training -- especially if one is training for 2-3 hours at a time -- some extra glycogen is likely to be quite useful.

    Loading is also persistent, at least in cyclists:

    "Thus, trained athletes’ supercompensated glycogen levels can remain higher than normal for up to 5 days post-loading."

    http://www.springerlink.com/content/jh9r7020q2857756/

    N.B. I wouldn't carb up after workouts if I were trying to cut weight for an event, both because not eating carbs after a workout forces one's body to refill its muscles via gluconeogenesis, and because supercompensated glycogen loading will involve putting on some water weight.

    EPOC
    My understanding is that hard workouts -- interval training, serious lifting, fighting, &c, but NOT chronic cardio -- cause sufficient damage to various tissues (muscle fibers, especially) that there are significant energy costs involved with repairs over the following 24-48 hours. (That is: building muscle has a non-zero metabolic overhead).
    “Most people do not do, but take refuge in theory and talk, thinking that they will become good in this way” -- Aristotle, Nicomachean Ethics, II.4
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    Posted On:
    3/17/2010 10:00pm

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    Hm.

    Quote Originally Posted by Jack Rusher View Post
    The research I've read suggests that there's no benefit in terms of protein synthesis (a long standing claim), but that post-workout carbs are good for recovery, including glycogen replacement, plus a spike in growth hormone and insulin.
    I was under the impression that the insulin spike was what drove the increased protein synthesis?

    Quote Originally Posted by Jack Rusher View Post
    My preference here is non-fructose (which will only replenish liver glycogen, not muscle), with an especial fondness for starches that degrade to glucose (e.g. bananas in a smoothie).
    I've been trying to sync up my schedule to hit up all-you-can-eat sushi immediately post-workout, but it's tough to get my friends in on it. Also, there's that whole pesky "showering" thing.

    Quote Originally Posted by Jack Rusher View Post
    This is probably the case for fight day
    I'd think that fifteen minutes (we can't all be Shane Carwin) would be right in the glycogen "breadbasket", so to speak. Actually, boosted muscular glycogen should be useful fairly early in the fight, what with both anaerobic and aerobic glycolysis kicking in depending on exertion.

    Quote Originally Posted by Jack Rusher View Post
    N.B. I wouldn't carb up after workouts if I were trying to cut weight for an event, both because not eating carbs after a workout forces one's body to refill its muscles via gluconeogenesis, and because supercompensated glycogen loading will involve putting on some water weight.
    How much of the former do you think is cortisol-related? Or more generally, how can we direct the gluconeogenesis to pick apart fats rather than protein?

    Latter should only apply in the last few days before a contest, no?

    Quote Originally Posted by Jack Rusher View Post
    My understanding is that hard workouts -- interval training, serious lifting, fighting, &c, but NOT chronic cardio -- cause sufficient damage to various tissues (muscle fibers, especially) that there are significant energy costs involved with repairs over the following 24-48 hours. (That is: building muscle has a non-zero metabolic overhead).
    This doesn't sound quite right. I can't find the actual study, but I think it's the one referred to in this quote:

    The dietary protein requirement for athletes has been a subject of debate for years, particularly for strength and power athletes. However, protein is important to the endurance athlete as well. Contrary to popular belief, recent research suggests that endurance athletes may actually require more protein than their resistance training counterparts. Tarnopolsky et al.[15] found that endurance athletes required approximately 1.4 grams of protein per kilogram of body weight to maintain nitrogen balance - a level higher than that needed by the resistance-trained subjects in the study.
    -Fink, Practical Applications in Sports Nutrition (p.368, emphasis mine)

    Steady-state cardio doesn't run up as big of an oxygen debt (so that compartment of EPOC is reduced), but it does do quite a bit in terms of catabolism.
    Quote Originally Posted by Emevas View Post
    Downstreet on the flip-flop, timepants.
  3. Jack Rusher is offline
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    Posted On:
    3/18/2010 10:24am


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    Quote Originally Posted by TheRuss View Post
    I was under the impression that the insulin spike was what drove the increased protein synthesis?
    That was the theory, but my understanding is that the effect is statistically insignificant in practice.

    Quote Originally Posted by TheRuss View Post
    I'd think that fifteen minutes (we can't all be Shane Carwin) would be right in the glycogen "breadbasket", so to speak.
    I was thinking of Bullshido readers, most of whom are either doing 5 minute BJJ matches or 3 * 2 minute kickboxing bouts.

    Quote Originally Posted by TheRuss View Post
    Or more generally, how can we direct the gluconeogenesis to pick apart fats rather than protein?
    A good question, but one on which I've not spent much time. The only time I've had any fat to get rid of was after ~9 months of supplementing with Weight Gainer shakes during a period of intense powerlifting. I didn't get stronger any faster than I normally do, but the sucrose-rich shakes did give me all the symptoms of early stage metabolic syndrome. Returning to the boxer's traditional diet of steak and salad melted off the pudge in no time.

    Quote Originally Posted by TheRuss View Post
    Latter should only apply in the last few days before a contest, no?
    Absolutely. I gulp down a whey + BCAA + banana shake after workouts, followed by a proper meal of meat & veg an hour or so later. In the week before an event I back off the shakes to drop the water weight easily.

    Quote Originally Posted by TheRuss View Post
    Steady-state cardio doesn't run up as big of an oxygen debt (so that compartment of EPOC is reduced), but it does do quite a bit in terms of catabolism.
    Study design is quite important here. The ones that apply an exercise protocol similar to most gym lifters come up with very different results than ones that study olympic lifters or trainees doing plyometrics. I won't be in the research library again for at least a week, but IIRC the 24-48 hour window difference in metabolic cost for the latter is something like 3:1 vs steady state running/cycling.
    “Most people do not do, but take refuge in theory and talk, thinking that they will become good in this way” -- Aristotle, Nicomachean Ethics, II.4
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    Posted On:
    3/18/2010 7:06pm

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    Quote Originally Posted by Jack Rusher View Post
    That was the theory, but my understanding is that the effect is statistically insignificant in practice.
    As in, "insulin spikes don't cause protein synthesis", or "insulin spikes after workouts don't cause any more protein synthesis than at other times"?

    Quote Originally Posted by Jack Rusher View Post
    I was thinking of Bullshido readers, most of whom are either doing 5 minute BJJ matches or 3 * 2 minute kickboxing bouts.
    Still, anaerobic glycolysis. IIRC, two minutes under a barbell can sap muscular glycogen reserves.

    Quote Originally Posted by Jack Rusher View Post
    Weight Gainer shakes
    Ugh.

    Quote Originally Posted by Jack Rusher View Post
    Study design is quite important here. The ones that apply an exercise protocol similar to most gym lifters come up with very different results than ones that study olympic lifters or trainees doing plyometrics. I won't be in the research library again for at least a week, but IIRC the 24-48 hour window difference in metabolic cost for the latter is something like 3:1 vs steady state running/cycling.
    I think you're talking about the overall energy balance here, which is convincingly linked to exercise intensity. I'm talking specifically about tissue damage, though.
    Quote Originally Posted by Emevas View Post
    Downstreet on the flip-flop, timepants.
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    Posted On:
    3/19/2010 8:29pm

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    I was going to make this post in another thread, but I think this one would be a better home for it.

    You don't use science to show that you're right, you use science to become right.
    -xkcd

    No matter how stupid and false an idea, a sufficiently motivated person can find support for it.
    Somewhere out there, there are anecdotes, essays, papers, studies and books that either support it or can be twisted to do so.
    This is good news for people who enjoy winning arguments, but not so good for people who are honestly trying to figure out what to do.

    ---

    The first principle is that you must not fool yourself--and you are
    the easiest person to fool. So you have to be very careful about
    that. After you've not fooled yourself, it's easy not to fool other
    scientists. You just have to be honest in a conventional way after
    that.
    -Richard P. Feynman

    There's an expression in my industry called "eating your own dog food".
    Much like these forums, this expression is about quality control - if your own product isn't good enough for you, you'd better fix it before you give it to anyone else.

    Well, when it comes to fitness and nutrition, I eat my own dogfood.
    I gather good information to the best of my abilities.
    I decide how to live based on this information.
    If my information is bad, I make bad decisions, and I suffer the consequences.
    With decisions like these, the consequences of bad decisions include injury, illness and death.

    All of a sudden, winning arguments on the Internet doesn't seem so important, does it?

    ---

    He who pays the piper calls the tune.
    -Proverb

    Even though there is no incentive for me to mislead myself, if I were a supplement salesman, or a professional trainer or nutritionist, or a published author, or a food producer, there would be incentive enough for me to mislead you.

    At the present time, I am none of these things, and I do not stand to make or lose any money based on what people believe about the issues discussed in this forum.

    I wish I didn't need to spell that out.

    ---

    As iron sharpens iron,
    so one man sharpens another.
    -Proverbs 27:17 NIV

    Bad information is a problem, but simply being told that you are wrong is not useful.
    Said information cannot simply be removed; it must be replaced with better information.

    Some environments encourage the propagation of good information.
    Others serve as breeding grounds for bad information.
    One of the most important "cleansers" of information is the appropriate use of citations.
    They transform a claim into an organ in a living body of knowledge by placing the research behind it into the larger context in which it was performed.

    This is why I am a stickler for sources, both for my own statements and those of others.
    They are not ammunition to win battles with.
    They are an opportunity to learn and improve.
    Quote Originally Posted by Emevas View Post
    Downstreet on the flip-flop, timepants.
  6. TheRuss is offline
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    Posted On:
    3/21/2010 5:47pm

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    In Experiment 1, young men (n=115) provided saliva samples before and after either conversing with a woman confederate or sitting alone for 15 min. Changes from baseline in salivary testosterone concentrations were significantly greater among the men exposed to women, but only among subjects tested in the afternoon. In Experiment 2, male subjects (n=99) interacted with either a male or a female confederate with saliva samples collected before and after these interactions and all experimental sessions conducted in the afternoon. Men who interacted with women exhibited significant elevations of testosterone relative to both their own baseline concentrations and to change scores among the men who interacted with other men. In addition, women confederates' ratings of men's extraversion and degree of self-disclosure were positively correlated with changes in testosterone. In both experiments, furthermore, changes in cortisol concentrations from baseline were significantly greater among men who spoke with women relative to men in the control conditions.
    -Roney et al., "Rapid endocrine responses of young men to social interactions with young women."

    Dammit.

    Edit: And also...

    The current experiment examined whether women show a similar endocrine response to physically and behaviorally attractive men. 120 women (70 naturally-cycling and 50 using hormonal contraceptives) were shown one of four 20-minute video montages extracted from popular films, depicting the following scenarios: 1) an attractive man courting a young woman (experimental stimulus), 2) a nature documentary (video clip control), 3) an unattractive older man courting a woman (male control), and 4) an attractive woman with no men present (female control). Saliva samples were taken before and after presentation of the stimulus, and were later analyzed for testosterone and cortisol content via enzyme immunoassay. Naturally-cycling women experienced a significant increase in both testosterone and cortisol in response to the experimental stimulus but to none of the control stimuli. Participants taking hormonal contraceptives also showed a significant cortisol response to the attractive man.
    -Lopez et al., "Attractive men induce testosterone and cortisol release in women."
    Quote Originally Posted by Emevas View Post
    Downstreet on the flip-flop, timepants.
  7. Jack Rusher is offline
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    Posted On:
    3/21/2010 5:56pm


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    Quote Originally Posted by TheRuss View Post
    As in, "insulin spikes don't cause protein synthesis", or "insulin spikes after workouts don't cause any more protein synthesis than at other times"?
    As in:

    The present study was designed to assess the impact of coingestion of various amounts of carbohydrate combined with an ample amount of protein intake on postexercise muscle protein synthesis rates. Ten healthy, fit men (20 ± 0.3 yr) were randomly assigned to three crossover experiments. After 60 min of resistance exercise, subjects consumed 0.3 g·kg–1·h–1 protein hydrolysate with 0, 0.15, or 0.6 g·kg–1·h–1 carbohydrate during a 6-h recovery period (PRO, PRO + LCHO, and PRO + HCHO, respectively). Primed, continuous infusions with L-[ring-13C6]phenylalanine, L-[ring-2H2]tyrosine, and [6,6-2H2]glucose were applied, and blood and muscle samples were collected to assess whole body protein turnover and glucose kinetics as well as protein fractional synthesis rate (FSR) in the vastus lateralis muscle over 6 h of postexercise recovery. Plasma insulin responses were significantly greater in PRO + HCHO compared with PRO + LCHO and PRO (18.4 ± 2.9 vs. 3.7 ± 0.5 and 1.5 ± 0.2 U·6 h–1·l–1, respectively, P < 0.001). Plasma glucose rate of appearance (Ra) and disappearance (Rd) increased over time in PRO + HCHO and PRO + LCHO, but not in PRO. Plasma glucose Ra and Rd were substantially greater in PRO + HCHO vs. both PRO and PRO + LCHO (P < 0.01). Whole body protein breakdown, synthesis, and oxidation rates, as well as whole body protein balance, did not differ between experiments. Mixed muscle protein FSR did not differ between treatments and averaged 0.10 ± 0.01, 0.10 ± 0.01, and 0.11 ± 0.01%/h in the PRO, PRO + LCHO, and PRO + HCHO experiments, respectively. In conclusion, coingestion of carbohydrate during recovery does not further stimulate postexercise muscle protein synthesis when ample protein is ingested.
    Coingestion of carbohydrate with protein does not further augment postexercise muscle protein synthesis
    (N.B. I'd like to see this done again with a bigger N).

    Quote Originally Posted by TheRuss View Post
    I think you're talking about the overall energy balance here, which is convincingly linked to exercise intensity. I'm talking specifically about tissue damage, though.
    I'm talking about both, actually. The quantity of muscle damage (and thus repair cost) isn't just damage/time (high time or high damage will get you there), but also how much of the body gets beaten up by the exercise.

    EDIT: I should mention that I'm using "muscle damage" in a way that might be confusing/misleading. My actual intent here is to refer to both damage/repair and other adaptation-related metabolic costs. The specifics of the latter processes are complicated and not fully understood, so I'm just tossing out short hand to avoid getting sidetracked.

    Lastly, to support my assertion above concerning damage/time, here's a paper showing that for identical total work HI vs LI is mostly similar in terms of MD markers, modulo creatine kinase concentration (higher at 24 hours for HI).
    Last edited by Jack Rusher; 3/21/2010 6:21pm at . Reason: Clarification.
    “Most people do not do, but take refuge in theory and talk, thinking that they will become good in this way” -- Aristotle, Nicomachean Ethics, II.4
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    Posted On:
    3/23/2010 12:27am

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    Quote Originally Posted by Jack Rusher View Post
    Aside from the N, it looks... okay. Ideally they'd have positive and negative nitrogen-balance controls to verify that their methodology would detect differences if they existed... but with ten subjects, that'd put them down at... two people per group.

    Also, those are some seriously bitch weights the subjects are moving. 3x10 on bench at 29kg? Ugh. Another reason to have positive and negative controls.

    I was suspicious about the glucose marker infusion given this...

    Even in the absence of carbohydrate coingestion, plasma insulin levels averaged 16.5 ± 1.6 µU/ml during the 6-h recovery period in the PRO treatment. Interestingly, it was recently suggested by Rennie et al. (27) that an increase in insulin levels above 10–15 µU/ml does not further enhance muscle protein synthesis and/or reduce protein degradation.
    ... but based on a glance at the numbers, I don't think a few micromoles of glucose per minute would make a difference.


    Quote Originally Posted by Jack Rusher View Post
    I'm talking about both, actually. The quantity of muscle damage (and thus repair cost) isn't just damage/time (high time or high damage will get you there), but also how much of the body gets beaten up by the exercise.

    EDIT: I should mention that I'm using "muscle damage" in a way that might be confusing/misleading. My actual intent here is to refer to both damage/repair and other adaptation-related metabolic costs. The specifics of the latter processes are complicated and not fully understood, so I'm just tossing out short hand to avoid getting sidetracked.
    IIRC, one of the selling features of HIIT is that they aren't as destructive as long-haul steady-state cardio - no cortisol buildup -> no chewing up muscle for energy. Maybe that's just part of the sales pitch, but it made sense at the time.

    Quote Originally Posted by Jack Rusher View Post
    Lastly, to support my assertion above concerning damage/time, here's a paper showing that for identical total work HI vs LI is mostly similar in terms of MD markers, modulo creatine kinase concentration (higher at 24 hours for HI).
    Ten sets of twelve reps requires an awfully loose definition of "high intensity". I prefer the following protocol:

    Bench press.
    Group 1: 14x45lbs
    Group 2: 2x315lbs

    I hesitate to say that some questions are too obvious to pay for a study to answer them, what with the whole conventional wisdom that heavier objects fall faster, but it'd just about knock me out of my chair if things were less clear-cut than they appear.

    ---

    And to answer one of my earlier questions:

    Quote Originally Posted by TheRuss View Post
    Or more generally, how can we direct the gluconeogenesis to pick apart fats rather than protein?
    Here's one shocker: lower-intensity exercise, in the "fat-burning zone", doesn't help.

    ... Muscle triglyceride lipolysis was stimulated only at higher intensities.... In recovery from high-intensity exercise, although the rate of lipolysis immediately decreased, the rate of release of fatty acids into plasma increased, indicating release of fatty acids from previously hydrolyzed triglycerides.
    -Romijn et al., "Regulation of endogenous fat and carbohydrate metabolism in relation to exercise intensity and duration"

    And here's another: eating less fat doesn't help either.

    2%FAT resulted in a 27% reduction (P < 0.05) in total fat oxidation vs. 22%FAT without altering the stable isotopically determined rates of plasma free fatty acid or glucose disappearance. Therefore, 2%FAT reduced calculated nonplasma FA oxidation by 40% in association with a 19% reduction in whole body lipolysis while increasing calculated minimal muscle glycogen oxidation compared with 22%FAT (all P < 0.05). In summary, an extremely low fat (2% of energy) and high-carbohydrate diet lowers whole body lipolysis, total fat oxidation, and nonplasma FA oxidation during exercise in the fasted state in association with a reduced concentration of intramuscular triglyceride.
    -Coyle et al., "Low-fat diet alters intramuscular substrates and reduces lipolysis and fat oxidation during exercise"

    But what about eating... more fat?

    This study determined the role of intramuscular triglyceride (IMTG) and adipose lipolysis in the elevated fat oxidation during exercise caused by a high-fat diet. In four separate trials, six endurance-trained cyclists exercised at 50% peak O2 consumption for 1 h after a two-day control diet (22% fat, CON) or an isocaloric high-fat diet (60% fat, HF) with or without the ingestion of acipimox, an adipose lipolysis inhibitor, before exercise. During exercise, HF elevated fat oxidation by 72% and whole body lipolysis [i.e., the appearance rate of glycerol in plasma (Ra glycerol)] by 79% compared with CON (P < 0.05), and this was associated with a 36% increase (P < 0.05) in preexercise IMTG concentration. Although acipimox lowered plasma free fatty acid (FFA) availability, HF still increased fat oxidation and Ra glycerol to the same magnitude above control as the increase caused by HF without acipimox (i.e., both increased fat oxidation 13–14 µmol·kg–1·min–1). In conclusion, the marked increase in fat oxidation after a HF diet is associated with elevated IMTG concentration and whole body lipolysis and does not require increased adipose tissue lipolysis and plasma FFA concentration during exercise. This suggests that altered substrate storage in skeletal muscle is responsible for increased fat oxidation during exercise after 2 days of an HF diet.
    -Zderic et al., "High-fat diet elevates resting intramuscular triglyceride concentration and whole body lipolysis during exercise"

    Nobody saw this coming!
    Quote Originally Posted by Emevas View Post
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  9. TheRuss is offline
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    Posted On:
    3/23/2010 11:46pm

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    Something I've been trying to nail down for a few days now...

    Peter at Hyperlipid said the following:

    Palmitic acid is the primary metabolic signal to switch from glucose burning to fat burning.
    I haven't been able to find any citations to this effect... actually, I've never heard anything like this before at all. Is this familiar to anyone else here?
    Quote Originally Posted by Emevas View Post
    Downstreet on the flip-flop, timepants.
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    Posted On:
    3/24/2010 12:41am

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    I'm going to have to read the references on this...

    SFA-induced chronic low-grade inflammation and insulin resistance in WAT affects other tissues and impairs their sensitivity to insulin, as well. SFA overflow from WAT is taken up by myotubes and hepatocytes, and accumulates in them. Similar to adipocytes, SFAs in myotubes activate signal transduction pathways through IKK and JNK, which causes serine phosphorylation and degradation of IRS-1 and desensitizes myotubes to insulin stimulation (35-38).
    -Funaki, "Saturated fatty acids and insulin resistance" (PDF)
    Quote Originally Posted by Emevas View Post
    Downstreet on the flip-flop, timepants.
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